Ethanol promotes protease activated receptor 1: Chemokine (C-X-C motif) receptor 4 heteromerization and enhances thrombin-induced impairment of human lung endothelial cell barrier function

被引：1
|
作者：
McGee, Michelle Y. [1 ]
Enten, Garrett A. [1 ]
Boshra, Sadia N. [1 ,2 ]
Ogunsina, Ololade [1 ]
Gaponenko, Vadim [3 ]
Gao, Xianlong [1 ]
Majetschak, Matthias [1 ,4 ]
机构：
[1] Univ S Florida, Morsani Coll Med, Dept Surg, Tampa, FL USA
[2] Univ S Florida, Dept Chem, Tampa, FL USA
[3] Univ Illinois, Dept Biochem & Mol Genet, Chicago, IL USA
[4] Univ S Florida, Morsani Coll Med, Dept Mol Pharmacol & Physiol, Tampa, FL USA
来源：
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2024年 / 1870卷 / 07期
基金：
美国国家卫生研究院;
关键词：
RESPIRATORY-DISTRESS-SYNDROME; ALCOHOL-CONSUMPTION; INJURY;
D O I：
10.1016/j.bbadis.2024.167335
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
- Ethanol enhances the propensity of PAR1 and CXCR4 to form heteromers.- Ethanol increases PAR1:CXCR4 heteromer expression in human lung microvascular endothelial cells (HULEC-5a).- Ethanol enhances the efficacy of PAR1 to activate G alpha 12 upon thrombin stimulation in cells co-expressing CXCR4.- Ethanol dose-dependently increases the efficacy of thrombin to impair HULEC-5a barrier function at clinically relevant concentrations.- Interference with PAR1:CXCR4 heteromerization mitigates effects of ethanol on thrombin-induced impairment of HULEC-5a barrier function.- Our findings provide a molecular mechanism that is likely to contribute to the increased risk of acute respiratory distress syndrome with alcohol abuse.
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页数：4
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